B o t u l i n u m Toxi n i n t h e

Treatment of Facial
Paralysis
Omid B. Mehdizadeh, MDa, Jacqueline Diels, OTb,
William Matthew White, MDc,*

KEYWORDS
 Synkinesis  Facial paralysis  Botulinum toxin  Asymmetry

KEY POINTS
 Combination treatment with neuromuscular retraining (NMR) exercises is essential for a better long-
term outcome.
 A sequence of first evaluation and treatment with NMR is recommended. When resistant muscle
groups are identified, treatment should be started with chemodenervation.
 Botulinum toxin can be injected in the affected synkinetic hemiface to relax hyperactive muscles
and the normal hemiface for balance to restore facial symmetry.
 Challenging areas for treatment of synkinesis include the midface and lip depressor complex and
should be addressed carefully.

INTRODUCTION satisfactory, they are invasive and irreversible.

Synkinesis makes up the overwhelming majority of
patients who present to a facial nerve center with
facial movement disorders. The synkinetic facial
movement can be subtle or completely disfiguring.
Interestingly, patients who have synkinetic activity
that is barely noticeable sometimes are the most
disturbed by the condition. Most patients begin to
see evidence of spastic activity of the facial muscles
6 months after recovery of their facial paralysis.
Rarely, this can even occur in the early phase of re-
covery as well. Synkinetic activity should only occur
on the hemifacial side of the original injury.
Restoration of permanent facial symmetry in
the postparalyzed synkinetic face has been a
mainstay of surgical treatment.1–4 Myectomy,
neurectomy, cross-face nerve grafts, and sling
procedures have all been implemented in
achieving outcomes. Although results can be
Botulinum toxin with and without neuromuscular
therapy has shown promising utility as a nonoper-
ative method in restoring normal facial features,
with recent literature demonstrating increasingly
long-term effects when used concurrently with
neuromuscular training.5–7
Produced by various strains of Clostridium
botulinum, multiple agents are currently available
on the United States market. There are currently
4 pharmacologic forms in the United States,
each with varying potencies and shelf lives: abo-
botulinumtoxinA (Dysport, Medicis Aesthetics,
Inc, Scottsdale, AZ; Azzalure, Galderma Labora-
tories, Lausanne, Switzerland), incobotulinumtox-
inA (Xeomin, Merz Aesthetics, Inc, Franksville,
WI), onabotulinumtoxinA (Botox, Allergan, Inc,
Irvine, C), and rimabotulinumtoxinB (Myobloc, Sol-
stice Neurosciences, LLC, Louisville, KY).8 Appli-
facialplastic.theclinics.com

cation remains percutaneous and intramuscular.

a
NYU Langone Medical Center, 550 First Avenue - NBV 5E5, New York, NY 10016, USA; b Facial Nerve Clinic,
UW Hospitals and Clinics, 600 Highland Avenue, Madison, WI 53792, USA; c NYU Ambulatory Care Center, 240
E 38th Street, 14th Floor, New York, NY 10016, USA
* Corresponding author.
E-mail address: William.white@nyumc.org

Facial Plast Surg Clin N Am 24 (2016) 11–20

http://dx.doi.org/10.1016/j.fsc.2015.09.008
1064-7406/16/$ – see front matter Ó 2016 Elsevier Inc. All rights reserved.
12 Mehdizadeh et al
Pattern of injection into muscle groups, units
administered, and frequency of treatment is not
standardized. Amounts administered have varied
from fractions of a unit per site9 to hundreds in
total,5,10,11 with increasing risk of adverse events
including oral incompetence, ptosis, diplopia,
exposure keratopathy, malaise, and worsened
cosmesis10,12 with larger doses. These events
are reversible, however, because the effects of
the toxin diminish.
Botulinum toxin continues to expand from its
first description in strabismus by Scott13 in 1980
to its eventual approval by the US Food and
Drug Administration for strabismus and blepharo-
spasm in 1989. Additional benefits were recog-
nized for aesthetic purposes by Carruthers and
Carruthers14 in their description of reduction in
glabellar frown lines in 1992.
Those who endure the sequela of postparalytic
synkinesis or abnormal involuntary facial move-
ments have been shown to have diminished qual-
ity of life, social interactions, peripheral visual
impairment, and a worsened self-impression of
personal appearance. In many instances, botuli-
num toxin therapy has been shown to decrease
the severity of these personal morbidities and
improve quality of life15 with validated methods
of subjective assessment including the Facial
Clinimetric Evaluation score,16 Sunnybrook Facial
Grading System,17 and Synkinesis Assessment
Questionnaire18 currently in use.
Characterized by involuntary movement in the
setting of volitional facial expressions, multiple
patterns have been described after facial nerve
injury including ocular, oral, and cervical synkine-
sias, dyskinesias, and hyperkesias. Typically, a
patient might experience spasm of the eye with
smiling or sometimes violent movements of the
corner of the mouth with eye closure. Manifesta-
tions of various forms require personalized injec-
tion patterns to achieve optimal outcomes and
aesthetics while minimizing side effects.5 The toxin
is typically administered to certain muscle groups
that provide certain function (ie, eye closure or
lip elevation) such as injection into the orbicularis
oculi, corrugators, and frontalis muscles for upper
synkinesias and zygomaticus, levator muscle
of upper lip, orbicularis oris, depressor labii,
depressor oris, and platysma muscles for lower
division defects.7,19 Functionally, botulinum toxin
chemically dennervates the neuromuscular junc-
tion by permanently blocking presynaptic acetyl-
choline release at the synaptic junction.
Mention of botulinum toxin A as an alternate
treatment of ocular synkinesia was first introduced
by Putternam20 in 1990. In his description of a sin-
gle case report, he discusses a 28-year-old woman
with “misdirection of the facial nerve” after Bell’s
Palsy causing ocular spasm with smiling.20 Since
then, the literature has been populated by
numerous studies augmenting the role of botulinum
toxin A in postparalytic facial synkine-
sia5,9–12,15,21–29 evolving to hints of long-term
improvement when used with concurrent neuro-
muscular training including half and whole face
mirror feedback6,7 and neuromuscular retraining
(NMR) therapy.26 The application of other tradi-
tional therapies in conjunction with botulinum toxin
has yet to be elucidated.
Causes of postparalytic facial synkinesia are
vast and varied, providing a universal platform for
this minimally invasive therapy. Central iatrogenic
tumor resections in the setting of vestibular and
facial schwannomas,27 middle ear surgery,24 as
well as peripheral parotid malignancies have
been described.27 Bells palsy and Ramsey Hunt
syndrome have also been implicated,9,19,27 in
addition to traumatic skull base injury.9
The neurophysiology of these involuntary move-
ments has yet to be fully understood. Aberrant
peripheral facial nerve regeneration is most
commonly attributed.30–32 However, studies in
the generation of synkinesis have demonstrated
predictable patterns of regeneration thought to
be owing to increased excitability within the facial
nucleus itself.33
This article reviews the current literature sup-
porting the use of botulinum toxin in producing
symmetric facial features and reducing unwanted,
involuntary movements. Methods, protocols, and
adverse events are discussed. Additionally, the
authors suggest that using botulinum toxin A ther-
apy in postparalytic facial synkinesis can provide
long-term results when used in conjunction with
other treatment modalities.
EVALUATION
Before beginning therapy, a patient should
undergo a thorough evaluation of their history of
facial paralysis and a complete evaluation of their
facial movements. Standardized photography and
video recording should be performed to clearly
document treatment efficacy. The 9 standard
views include face at rest, brow elevation, com-
plete eye closure, nose wrinkling, grin, full smile,
pucker, whistle, and lower lip depression.
It is important during the evaluation to identify
the “triggers” for eliciting the synkinesis. This
most commonly is forceful eye closure or a puck-
ering movement of the lips. Critical to the evalua-
tion, the patient should be questioned their main
concerns are and what areas of the face and
neck are the most troubling. Patients typically
 Treatment of Facial Synkinesis 13

remark about the discomfort of spasms around the is no precedent for identifying and understanding
eye or neck. Ideally, these areas should be ad- it. When muscles contract out of sequence, the
dressed first and foremost. It is recommended to facial skin is displaced in an unusual direction,
wait at least 6 months after the onset of facial pa- creating a distorted expression. What seems to
ralysis to allow recovery. Any intervention before be lack of movement caused by weakness
that time can potentially make the synkinesis may in fact be abnormal hyperactivity of an
worse. opposing muscle restricting range of motion
Ideally, the patient should have an initial treat- and excursion.
ment by a physical or occupational therapist who Comprehensive retraining incorporates signifi-
has specific training in facial NMR. It is helpful for cant education regarding facial anatomy and mus-
the physician to evaluate the patient before begin- cle actions. This is key to comprehending the true
ning therapy, which can help to determine the nature of the disability, that is, the difference be-
progress of treatment. A team approach can be tween a deficiency of muscle activity resulting in
very helpful to the patient. no movement (flaccidity) and aberrant muscle ac-
tivity (synkinesis) resulting in wrong movement. In
THERAPEUTIC OPTIONS
Neuromuscular Retraining
Facial NMR is a specific subset of occupational
and physical therapy developed for improving
motor learning and functional outcomes in patients
with facial paralysis, paresis and/or synkinesis af-
ter facial nerve injury. Facial NMR techniques are
based on characteristics unique to the facial nerve
and muscles it innervates (eg, lack of muscle
spindles and presence of emotional, as well as
volitional, neural inputs).34 Facial NMR should not
be confused with the more common, nonspecific
therapies that promote gross motor, maximum
effort exercises and electrical stimulation, both of
which are contraindicated in facial paralysis.35
Rather, NMR focuses on providing sensory infor-
mation to enhance neural adaptation and learning
via the practice of minimal, precisely coordinated
movement patterns in conjunction with modalities
such as surface electromyographic, propriocep-
tive, and mirror feedback. This comprehensive
clinical program was first described by Balliet
and colleagues36 in 1982, who reported improved
function in patients more than 2 years after facial
nerve injury. Acquisition of new motor behaviors
was attributed to brain plasticity, the capacity of
Fig. 1. Muscles of facial expression (arrows depict
the central nervous system to modify its organiza- normal direction of contraction). Muscles: BUC, bucci-
tion, resulting in lasting functional change.36 nators; COM, compressor naris; COR, corrugator;
From a nonoperative rehabilitation perspective, DAO, depressor anguli oris; DIN, dilator naris; DLI,
facial muscles play a different role than other mus- depressor labii inferioris; FRO, frontalis; LAO, levator
cles in the body. Simply stated, their purpose is to anguli oris; LLA, levator labii alaeque nasi; LLS, levator
move the facial skin in various directions, produc- labii superioris; MEN, mentalis; OCI, orbicularis oculi
ing a wide variety of expressions used primarily for inferioris; OCS, orbicularis oculi superioris; OOI, orbi-
nonverbal communication, eye closure, and oral cularis oris inferioris; OOS, orbicularis oris superioris;
PLA, platysma; PRO, procerus; RIS, risorius; ZYJ, zygo-
motor functions. The subtleties of human expres-
maticus major; ZYN, zygomaticus minor. Facial nerve
sion require a delicate balance of activity among
branches: B, buccal; C, cervical; M, mandibular; T, tem-
multiple facial muscles. The presence of synkine- poral; Z, zygomaticus. (Adapted from Balliet R. Facial
sis destroys the normal balance. paralysis and other neuromuscular dysfunctions of the
Synkinesis is the most common condition peripheral nervous system. In: Payton OD. Manual of
treated by the facial NMR therapist. Because it physical therapy. New York: Churchill Livingstone;
does not occur in other areas of the body, there 1989. p. 179; with permission.)
14 Mehdizadeh et al
cases of synkinesis, the common practice of pre-
scribing maximum effort movements (in an erro-
neous attempt to strengthen muscles) intensifies
the abnormal response, reinforcing the synkinesis.
Appropriate intervention focuses on accurately
coordinating viable, albeit synkinetic, muscles
rather than stimulating flaccid ones. With skilled
training it is possible to improve movement pat-
terns and expression even many years after synki-
nesis develops.35,36
When used in conjunction with facial NMR, bot-
ulinum toxin provides a “window of opportunity”
during which the patient can learn and practice
isolated, coordinated movement patterns without
the cocontraction and restriction caused by synki-
nesis. It is preferable to complete 6 months of re-
training before injecting botulinum toxin to enable
the patient to learn the synkinesis inhibition tech-
niques. The presence of botulinum toxin before
retraining does not afford this same learning
opportunity.
The retraining therapist, as part of the multidisci-
plinary team, is instrumental in precisely identi-
fying the synkinetic muscles most restricting
normal function. These, when injected, should
allow for greater ease and range of motion in
Fig. 2. Treatment of Synkinesis in the Peri-Ocular Area. (A) Patient with visible synkinesis in the right orbicularis
oculi muscle. Botulinum toxin was injected in the right periorbital area displayed in the figure (doses are in Units,
Black 5 1cc dilution). (B) One month after botulinum treatment showing improved eye opening.
keeping with the patient’s stated goals, without
causing additional morbidity. Targeting the most
appropriate injections sites for the best outcome
is challenging owing to the complex interactions
of the facial muscles. Knowledge of anatomy is
not enough. It is also essential to know the working
action of each muscle, both in isolation and in
conjunction with the actions of others.
The most common injection sites include the or-
bicularis oculi, corrugator, platysma, and mentalis
muscles (Fig. 1). Recently, minimal dose injections
to the synkinetic buccinator have proven to be of
benefit in improving outcomes.37 The midfacial
muscles are rarely injected to avoid creating weak-
ness in key areas targeted during the NMR pro-
cess, such as smile. For greatest accuracy in
targeting injection sites, the patient is asked to
demonstrate the expressions that elicit the synki-
netic response. Forceful eye closure, smile,
pucker and snarl will most commonly produce
the response. Each movement may elicit a unique
synkinetic pattern, so all should be tested. It is
important to note that even a region demonstrating
little to no volitional activity (e.g. forehead) can
demonstrate significant aberrant activity in a syn-
kinetic pattern, so should be evaluated in that
 Treatment of Facial Synkinesis 15

context. (In such a case, no brow movement is
observed when the patient attempts to raise it voli-
tionally, however, significant elevation may occur
during smile or pucker).
Neuromodulator Injection
When the botulinum toxin vials arrive, they are
frozen and need to be reconstituted with normal
saline. The authors use 2 main preparations of
botulinum toxin, a 1 mL dilution (10 units per
each 0.1 mL) and a 2 mL dilution (5 units per
each 0.1 mL). The 1 mL dilution provides a solution
that allows a more targeted approach to muscle
relaxation, particularly in the medial midface zygo-
matic complex and the periocular areas. The 2 mL
dilution allows for much greater diffusion of the
toxin, and can be advantageous in larger muscles,
such as the platysma.
After the injection, patients should avoid any
physical activity or facial exercises for 2 days to
prevent diffusion of the product to unwanted areas.
Botulinum toxin starts to take effect in 3 to 5 days
and the peak effect is routinely seen at 2 weeks.
For that reason, we usually recommend that pa-
tients follow up 1 month after treatment to assess
efficacy of the treatment. At that point, any addi-
tional areas that did not respond as well as desired
can be treated with additional botulinum toxin. It is
highly recommended to begin conservatively with
the patient’s first treatment, and then titrate the bot-
ulinum toxin dose upward as needed.
on the nasolabial fold can result in the lack of func-
tion of the smiling muscles and cause great distress
to patients for 3 to 4 months until the effect of the
drug wears off. Patients most often state that they
would prefer the increased muscle tension, rather
than looking “paralyzed,” with complete muscle
inactivity. For this reason, NMR is a critical aspect
to address tension in the cheek. Neuromuscular re-
taining can often be a safer, much more effective
intervention than botulinum toxin injection in
relieving the painful spasm in the cheek.
Occasionally, one can elicit spasm in the area of
the zygomaticus minor muscle, located in the na-
solabial fold just about one-third of the distance
from the nasal ala to the lateral commissure
(Fig. 3). A precise injection of botulinum toxin of
0.5 to 1 unit, with a concentrated 1 mL dilution of
product to minimize diffusion, can be very effec-
tive. Injecting over the malar eminence high and
lateral in the cheek is not recommended because
this leads frequently to complete weakness of
the zygomatic muscle complex.
Perioral The most frequent complaint that we
hear from patients is the inability to achieve what

Periocular
The forehead and periocular area contains the
muscles that both elevate and depress the brow
complex. The frontalis muscle is the main elevator
of the eyebrows, and the corrugator supercilli and
orbicularis oculi are the main depressors of the
eyebrows. Spasm of the frontalis and corrugator
supercilli muscles are frequent causes of tension
headache pain in synkinesis patients, and can
often be elicited with a careful history and exami-
nation. Additionally, one of the most frequent com-
plaints of patients with synkinesis is the tight
spasm that can occur in the orbicularis oculi mus-
cle. This causes a narrowing of the visual field in
the effected eye, painful spasm of the muscle,
and exaggeration of the crow’s feet area (Fig. 2).
Midface One of the most challenging areas to inject
is the cheek and midface area, because spasm of
Fig. 3. Spasm of the Zygomaticus Minor. (A) In the
the zygomatic muscles leads to pain and discom-
right hemi-face, forceful eye closure triggers spasm
fort in the cheek. Unfortunately, this is the area of the right Zygomaticus Minor muscle. Botulinum
that is most frequently cited by patients as being toxin was injected in the area just anterior to the right
the most bothersome in terms of pain and discom- nasolabial fold displayed in the figure (doses are in
fort. The lower face is also the most challenging Units, Black 5 1cc dilution). (B) One month following
area to inject. Overinjection of the muscles acting treatment, there is reduced spasm in the right cheek.
16 Mehdizadeh et al

they know as a normal smile. This can be caused
by a variety of factors including the downward pull
of lip depressor muscles that prevent lateral up-
ward excursion of the lateral commissure. Tar-
geted treatment of the platysma, depressor labi
inferioris, and depressore anguli oris is quite help-
ful. Symmetry of the lower lip, particularly during
smiling is very important, and injection of the
contralateral lip depressor muscles can often be
helpful.
A typically overlooked muscle that can limit
lateral excursion of the smile is the buccinator mus-
cle (Fig. 4). The Buccinator muscle is an accessory
muscle for mastication, but is controlled by the
buccal branch of the facial nerve. The muscle’s
main action is to pull the lateral commissure of
the mouth posteriorly and to tense and flatten the
mucosal surface of the cheek against the teeth. In
doing so, the angle of the mouth is pulled closed.
Spasm of the buccinator muscle pulls the corner
of the mouth posteriorly on the synkinetic side,
limiting exposure of the upper teeth and upward
movement of the smile.
Neck
Tense spasm of the platysma muscle on the
affected side is a freqent complaint among synki-
nesis patients. The medial fibers contribute to the
depressor function of the lateral oral commis-
sure, and can act as a pulley that pulls the corner
of the mouth in a downward direction. This
downward traction of the platysma muscle inter-
feres with smiling as it acts against the zygomatic
muscles to allow upward and lateral excursion of
the oral commissure. As a result, after treating
the platysma muscle with botulinum toxin, pa-
tients usually report improvement in their ability
to smile on the affected side. Typical injection
doses in the platysma muscle are 15 to 20 U of
botulinum toxin (Fig. 6). We typically use 2 cc di-
lutions to facilitate even spread of the drug within
the muscle.

Fig. 4. Synkinesis of the buccinator muscle. (A) Simulation of buccinator spasm and the effect on the oral commis-
sure. This patient had left facial synkinesis, with image (B) displaying the normal, unaffected side. Compare to (C),
showing synkinetic muscular activity upon forcefull eye closure. Note the spasm and bulge of the buccinator
muscle.
 Treatment of Facial Synkinesis 17

Contralateral Normal Side: Addressing

Asymmetries
In many patients, the perception of asymmetry can
be the most troubling to them, and can be very
bothersome during normal conversation. The 2
most common offenders are the periocular and
lateral commissure. Overactivity in these areas dur-
ing laughing or conveying emotions can amplify
and draw attention to the patient’s facial asymme-
try. Both young and old patients are affected, but
age related changes amplify this effect.
When addressing the synkinetic hemiface with
botulinum injections, the contralateral normal cor-
rugator and orbicularis oculi are also addressed.
This can reduce the appearance of an unsightly
bulge of the corrugator muscle and crow’s feet
on the normal side. It is also very important to
consider the position of the patient’s eyebrows
on the normal side. Increased resting tone of the
depressor muscles on the affected synkinetic
side can cause the eyebrow to be positioned
lower. Therefore, the eyebrows can be evened
out by placing a relatively lower dose of botulinum
toxin on the normal side, and a higher dose on the
synkinetic spastic side. The same concept can be
Fig. 5. Platysma Muscle Synkinesis. Treatment of
applied where increased resting tone of the fronta- Synkinesis in the Peri-Ocular Area. (A) Patient with
lis causes the eyebrow to be higher on the affected visible synkinesis in the right Platysma muscle trig-
synkinetic side. gered by lip puckering. Botulinum toxin was injected
Abnormalities of the smile can be one of the into neck displayed in the figure (doses are in Units,
most frequent complaints in patients with synkine- Yellow 5 2cc dilution). (B) One month after botuli-
sis. Patients with a full denture smile, as described num treatment showing improved eye opening.
by Rubin,37,38 can be particularly susceptible.
Overpull of the zygomatic muscles that elevate patients typically require a higher dose than
the lateral commissure, and the depressor anguli the common cosmetic patient. Some of the
oris and depressor labii inferioris that depress the more common risks include slight bruising after
lip, can greatly exaggerate the asymmetries during injections.
smiling or laughing. Injecting botulinum toxin in the
zygomatic elevator muscles is a slippery slope,
and must be done with great trepidation. Dosing ALTERNATIVE TREATMENTS
is typically done with 0.5 to 1 unit just lateral to
Treatment of synkinesis with botulinum toxin is
the oral commissure.
relatively easy, requires no downtime for the pa-
Botulinum injection in the contralateral lip
tient, and is quite reproducible. For this reason,
depressor muscles can help produce a dramatic
botulinum toxin injection has become the standard
improvement in the symmetry of the smile
of care for patients with synkinesis. Neurolysis has
(Fig. 5). It is important, however, to diagnose
experienced a return to practice, and this proce-
whether the overactive downward pull is owing
dure was historically once the main treatment for
to the depressor labii inferioris, depressor anguli
synkinesis. Selective mymectomy has been an
oris, or both. The depressor anguli oris is a broader
alternative treatment for a more permanent relief
muscle that typically requires a greater dosage
of synkinesis. Mymectomy has been offered for
(3–5 U) than its more medial counterpart depressor
many of the facial muscles, but may be the most
labii inferioris (1–3 U).
effective for overcontraction of the stapedius mus-
cle, causing a loud irritating noise from movement
Risks of the tympanic membrane with facial movement.
Botulinum toxin treatment is very well-tolerated The most common mymectomy performed today,
and has minimal risks to the patient. Care should however, is transection of the platysma muscle
be taken, however, because facial paralysis (Fig. 6), performed through a 2-cm incision in a
18 Mehdizadeh et al

neck crease. A history of relief of pain and discom-
fort from synkinesis with botulinum toxin injections
is usually a good predictor of a successful
mymectomy.
FUTURE DIRECTIONS
One of the downsides of neuromodulator treat-
ment of synkinesis is that injections must be
repeated every 3 months. Second, injections are
performed with very small needles and are quite
well-tolerated; however, there is some discomfort
associated with the treatment. One new pharma-
ceutical company, Revance Therapeutics, has
developed new neuromodulators to address
some of these issues.
The first product, RT001, is a topical gel formu-
lation of the botulinum toxin type 1.39 The drug is
applied to the skin at precise locations, and after
sufficient time is absorbed and delivers its effect.
The company is targeting a cosmetic indication
for crow’s feet lines. The drug has shown prom-
ising results in more than 17 clinical studies and
is currently in phase III clinical trials. Topical
RT001 has not been studied in synkinesis, but it
seems ideally positioned to address synkinetic
facial muscles that located more superficially in
the facial soft tissues, such as the orbicularis oculi
and orbicularis oris. A superficial location and
nearby proximity to the skin would theoretically
minimize the distance for absorption and have a
greater chance of success.
The second product, RT002, is a new injectable
formulation of the botulinum toxin that was de-
signed to offer a more target delivery of the botu-
linum toxin and reduce the spread of toxin
beyond the site of injection.40 Again, RT002 has
not been studied in synkinesis patients, but seems
ideally suited to precisely target a facial muscle in
spasm, while sparing a nearby, uninvolved mus-
cle. RT002 has currently completed phase II clin-
ical trials for cosmetic glabellar frown lines and
functional cervical dystonia. One encouraging
finding from the clinical studies was that RT002
achieved a median duration effect of 7 months.
The longer duration of effect might reduce the
number of visits that synkinesis patients typically
need.

Fig. 6. Injection of contralateral lip depressors improves the smile. (A) Patient with visible synkinesis in the left
hemiface, botulinum toxin was injected into the affected left face, and the contralateral right lip depressors
(doses are in Units, Black 5 1cc dilution; Yellow 5 2cc dilution). (B) One month after botulinum treatment
showing a balanced smile.

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